Ka. Albarazanji et Rj. Balment, RENAL,ENDOCRINE AND VASCULAR EFFECTS OF ATRIAL-NATRIURETIC-PEPTIDE INA NOVEL VASOPRESSIN-DEFICIENT GENETICALLY HYPERTENSIVE STRAIN OF RAT, Experimental physiology, 80(2), 1995, pp. 275-284
In the absence of the potentially confounding influence of vasopressin
in hypertension, the effects of atrial natriuretic peptide (ANP) on a
rterial blood pressure and renal handling of water and sodium were ass
essed from comparison of responses to intravenous ANP infusion in anae
sthetized vasopressin-deficient New Zealand genetically hypertensive (
DI/H) rats and their normotensive substrain (DI/N). After 320 min of h
ypotonic saline infusion, plasma ANP concentration was significantly h
igher in DI/H compared with DI/N rats. ANP administration increased ci
rculating ANP concentration in both groups. Plasma angiotensin II conc
entration was higher in DI/H than in DI/N rats; infusion of ANP raised
circulating angiotensin II in both groups though this achieved statis
tical significance only in DI/N rats. Plasma aldosterone concentration
s were initially similar in normotensive and hypertensive animals and,
in both, were reduced markedly by i.v. ANP infusion. Administration o
f ANP produced sustained hypotension in both groups. However, the hypo
tensive effect of ANP was more pronounced in DI/H compared with DI/N r
ats. Heart rate was initially similar in the two groups, and infusion
of ANP produced no detectable change. By comparison with animals maint
ained on hormone-free infusate, urine flow increased markedly over the
80 min period of ANP infusion in both groups, by 142 % in DI/H rats a
nd 127 % in DI/N rats. ANP administration produced a natriuresis in bo
th groups but the increase in Na+ excretion was much greater in DI/H (
342 %) than in DI/N (139 %) rats. It appears from the current study th
at vasopressin-deficient hypertensive rats are more sensitive to ANP w
ith regard to effects on blood pressure and renal excretion than their
vasopressin-deficient normotensive substrain. These differences may,
in part, reflect adjustments to long-term elevation in blood pressure
and in plasma ANP concentration in hypertension and, in part, rely on
the associated disturbances in related endocrine systems.